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  • Title: p19(ras) amplifies p73beta-induced apoptosis through mitochondrial pathway.
    Author: Kim JW, Kim WH, Jeong MH, Jang SM, Song KH, Park SI, Song PI, Kang KH, Choi KH.
    Journal: Biochem Biophys Res Commun; 2008 Aug 15; 373(1):146-50. PubMed ID: 18555006.
    Abstract:
    p73 and p53 have been known to play an important role in cellular damage responses such as apoptosis. Although p73 is a structural and functional homolog of p53 tumor suppressor gene, much less is known about the mechanism of p73-induced apoptotic cell death. In this study, we demonstrate that p19(ras) interaction with p73beta amplifies p73beta-induced apoptotic signaling responses including Bax mitochondrial translocation, cytochrome c release, increased production of reactive oxygen species (ROS) and loss of mitochondrial transmembrane potential (DeltaPsi(m)). Furthermore, endogenous expression of p19(ras) and p73beta is significantly increased by Taxol treatment, and Taxol-enhanced endogenous p73beta transcriptional activities are further amplified by p19(ras), which markedly increased cellular apoptosis in p53-null SAOS2 cancer cell line. These results have important implications for understanding the molecular events of p19(ras) to p73 functions in cancer cells.
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